Date: 2014-09-29
Type of information: Presentation of results at a congress
phase: preclinical
Announcement: presentation of results at the 3rd International Conference on Immune Tolerance, being held in Amsterdam, the Netherlands, from September 28-30, 2014
Company: Compugen (Israel)
Product: CGEN-15001
Action
mechanism: CGEN-15001 is a novel Fc fusion protein drug candidate for autoimmune diseases, consisting of the fusion of the extracellular region of CGEN-15001T to an IgG Fc domain. CGEN-15001T is a novel immune checkpoint discovered by Compugen through its predictive discovery infrastructure. CGEN-15001 was shown to be effective in treating several autoimmune diseases in animal models, including models of multiple sclerosis, rheumatoid arthritis, psoriasis and type 1 diabetes. In preclinical models, CGEN-15001 treatment has been shown to induce a durable long-term response suggestive of immune tolerance restoration. CGEN-15001 has also promoted graft survival in a model of bone marrow transplantation. Further research demonstrated that CGEN-15001 has an immune modulatory function attenuating inflammatory responses and promoting regulatory anti-inflammatory activity, including the promotion of regulatory T cells.
Disease:
Therapeutic area: Autoimmune diseases
Country:
Trial details:
Latest
news: * On September 29, 2014, Compugen announced that experimental results supporting CGEN-15001’s induction of long-term autoimmune disease remission in disease animal models, potentially through a novel mechanism of action, are being presented at two sessions at the 3rd International Conference on Immune Tolerance, being held in Amsterdam, the Netherlands, from September 28-30, 2014. The presentations are being given by Joseph R. Podojil, PhD, of Northwestern University Feinberg School of Medicine, and by Iris Hecht, PhD, Principal Scientist at Compugen.
In a poster presentation titled “Tolerogenic and immunomodulatory effects in the EAE model of multiple sclerosis induced by CGEN-15001, an Fc-fused protein derived from a novel immune checkpoint,” Dr. Podojil disclosed data indicating that the durable therapeutic responses to CGEN-15001 treatment, demonstrated in disease animal models, are potentially maintained via regulatory T cells (Tregs), which are known to play critical roles in the maintenance of immune tolerance. These initial results were recently generated as part of Compugen’s collaboration with Prof. Stephen D. Miller, Professor of Microbiology-Immunology at Northwestern University Feinberg School of Medicine, where Dr. Podojil is a Research Assistant Professor in Prof. Miller’s research group.
The recent experimental results being disclosed by Dr. Podojil are based on the R-EAE mouse model of multiple sclerosis, in which short-term administration of CGEN-15001 results in long-term disease remission. The inactivation of Tregs in CGEN-15001 treated R-EAE mice during the disease remission period resulted in disease relapse, strongly suggesting that Tregs are essential for maintenance of CGEN-15001’s long-term therapeutic effect. Additional experimental results in the R-EAE model presented by Dr. Podojil, using blockade of central pathways for Treg induction and function, further support involvement of Tregs in the in vivo mechanism of action of CGEN-15001.
